Biomedical subjects

O Z Chi

Publications and source records attributed to O Z Chi.

At least 37 records · Page 2Linked to original sources

PubMed1996

Cerebral microregional oxygen balance during chronic versus acute hypertension in middle cerebral artery occluded rats.

This study was performed to compare microregional 0(2) supply and consumption balance in spontaneously hypertensive rats (SHR), normotensive Wistar Kyoto rats (WKY), and in phenylephrine-induced acutely hypertensive WKY (WKY + ph) rats. Under isoflurane anesthesia, a middle cerebral artery (MCA) of SHR (n = 7) and WKY (n = 14) rats was occluded. Seven of the WKY rats were infused with phenylephrine (WKY + ph) to keep the mean arterial pressure (MAP) at the same level as that of the SHR. In all animals, 1 h after MCA occlusion, regional cerebral blood flow (rCBF) was determined using an autoradiographic technique, and microregional arterial and venous 02 saturations were determined using microspectrophotometry. MAP was 76 +/- 4 (SD), 136 +/- 15, and 132 +/- 12 mm Hg for the WKY, WKY + ph, and SHR groups, respectively. All variables describing regional O2 balance and rCBF were similar between the SHR and the WKY groups in the ischemic cortex as well as in the contralateral cortex. With phenylephrine infusion, rCBF of both the ischemic cortex and the contralateral cortex were increased in the WKY group. The average 02 supply-to-consumption ratio in the ischemic cortex was higher in the WKY + ph than in the WKY or SHR group. In the ischemic cortex, heterogeneity of venous 02 saturation (SvO2), expressed as a coefficient of variation (CV = 100 X SD/mean), was significantly lower in the WKY + ph (18.3 +/- 2.4) group than in the SHR (30.5 +/- 11.8) or in the WKY (31.3 +/- 9.0) group. The number of veins with low 02 saturation (SvO2 < 40%) in the ischemic cortex was significantly lower in the WKY + ph than in the SHR or in the WKY group. Our data suggest that in chronically hypertensive animals, cerebrovascular adaptations enable the microregional 02 balance in focal ischemia to be maintained at a level similar to that of normotensive animals. However, in normotensive animals with focal cerebral ischemia, an acute increase of MAP improves microregional O2 balance.

Acute Disease↗

PubMed1996

Hydroxyethyl starch solution attenuates blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats.

This study was performed to investigate whether a fraction of hydroxyethyl starch macromolecules, prepared from pentastarch and known as "Hes-Pz," with molecular weights of 100,000-1,000,000, protects against blood-brain barrier (BBB) disruption due to intracarotid injection of hyperosmolar mannitol. Rats were anesthetized with isoflurane, and retrograde catheterization of a unilateral eternal carotid artery was performed. Except for the Control group (n = 8), hemodilution was performed using lactated Ringer's solution LR group, n = 7), 6% hetastarch (HES group, n = 7), or 6% HES-Pz (HES-Pz group, n = 8) to reduce the hematocrit to about 23%. The BBB transfer coefficient (Ki) of 14C-alpha-aminoisobutyric acid was determined after a unilateral intracarotid injection of 25% mannitol. Blood pressure and hematocrit were similar in all groups. In the control group, Ki was increased significantly in the ipsilateral cortex (IC) where mannitol was injected (16.3 +/- 6.1 vs 4.1 +/- 1.4 microL.min-1) when compared with the contralateral cortex (CC). Ki was similar in the CC in all four groups. The Ki in the IC was significantly lower in the HES-Pz(6.4 +/- 3.5 microL.g-1.min-1) than in the Control, HES, or LR group (16.3 +/- 6.1, 19.0 +/- 12.9, 17.9 +/- 10.8 microL.g-1.min-1, respectively). Our data suggest that HES-Pz significantly attenuates disruption of the BBB caused by an injection of hyperosmolar mannitol.

Aminoisobutyric Acids↗

PubMed1996

Increased blood-brain permeability with hyperosmolar mannitol increases cerebral O2 consumption and O2 supply/consumption heterogeneity.

This study was performed to evaluate whether increasing the permeability of the blood-brain barrier by unilateral intracarotid injection of hyperosmolar mannitol would alter O2 consumption and the O2 supply/consumption balance in the ipsilateral cortex. Rats were anesthetized with 1.4% isoflurane using mechanical ventilation. Retrograde catheterization of a unilateral external carotid artery was performed to administer 25% mannitol at a rate of 0.25 ml/kg/s for 30 s. The blood-brain barrier transfer coefficient (K(i) of 14C-alpha aminoisobutyric acid was measured in one group (N = 7) after administering mannitol. Regional cerebral blood flow (rCBF), regional arterial and venous O2 saturation and O2 consumption were measured in another group using a 14C-iodoantipyrine autoradiographic technique and microspectrophotometry (N = 7). Vital signs were similar before and after administering mannitol. K(i) was significantly higher in the ipsilateral cortex (IC) (22.3 +/- 8.4 microliters/g/min) than in the contralateral cortex (CC) (4.4 +/-1.1). rCBF was similar between the IC (105 +/- 21 ml/g/min) and the CC (93 +/- 20). Venous O2 saturation was lower in the IC (43 +/- 7%) than in the CC (55 +/- 4%). The coefficient of variation (100 x SD/mean) of venous O2 saturation was significantly elevated in the IC (32.3) compared with the CC (18.2), indicating increased heterogeneity of O2 supply/consumption balance. O2 consumption was higher in the IC (9.6 +/- 3.0 ml O2/100 g/min) than in the CC (6.7 +/- 1.5). Our data suggested that increasing permeability of the blood-brain barrier increased cerebral O2 consumption and the heterogeneity of local O2 supply/consumption balance.

Animals↗

PubMed1995

Effects of CAS 754, a new nitric oxide donor, on regional cerebral blood flow in focal cerebral ischemia.

Nitric oxide (NO) plays an important role in regulating regional cerebral blood flow (rCBF). This study was performed to compare the effects of the NO donor, CAS 754, a sydnonimine derivative, and sodium nitroprusside (SNP) on rCBF in ischemic and nonischemic brain regions. Twenty-eight rats were anesthetized with 1.4% isoflurane and were mechanically ventilated. A middle cerebral artery (MCA) was occluded in each animal. In the CAS 754 group (n = 7), 40 min after MCA occlusion, 4-6 mg/kg of CAS 754 was administered intravenously (i.v.) to decrease the mean arterial blood pressure (MAP) to 55-60 mm Hg. In the SNP group (n = 7), an infusion of SNP was started to decrease the MAP to the same level as that of the CAS group. In the CAS-Ph group (n = 7), phenylephrine was infused after CAS754 had been administered in order to maintain the MAP at the control level (95-100 mm Hg). The remaining seven rats were used as a control group. rCBF was measured using 14C-iodoantipyrine in all four groups of animals 1 h after MCA occlusion (20 min after the start of drug administration). The average rCBF of the nonischemic brain regions (121 +/- 15 mL.min-1.100 g-1) was increased by 34% with CAS 754 (162 +/- 39 mL.min-1.100 g-1). However, SNP did not significantly change the average rCBF of the nonischemic brain regions (114 +/- 5 mL.min-1.100 g-1). Neither CAS 754 nor SNP significantly affected the rCBF of the ischemic cortex (control 51 +/- 7, CAS 61 +/- 13, SNP 53 +/- 18 mL.min-1.100 g-1). Phenylephrine infusion in the CAS 754-treated animals did not significantly affect the rCBF of the ischemic or nonischemic brain regions. In conclusion, our study demonstrated that CAS 754 was a more effective cerebral vasodilator than nitroprusside when administered systemically. In the ischemic cortex, neither CAS 754 nor nitroprusside improved rCBF Failure of CAS 754 to improve the rCBF of the ischemic cortex does not appear to be due to hypotension induced by CAS 754.

Animals↗

PubMed1994

Effects of topical methylene blue on cyclic GMP level, blood flow, and O2 consumption in focal cerebral ischaemia.

We hypothesized that a decrease in cyclic GMP, a second messenger in the glutamate-nitric oxide pathway, would reduce oxygen consumption and improve O2 balance in the ischaemic cerebral cortex. To test this hypothesis, a study was performed in unilateral middle cerebral artery occluded rats which were assigned to either a control or methylene blue (10(-3) M) group. Regional cerebral blood flow was determined using 14C-iodoantipyrine and regional arterial and venous O2 saturations were determined by microspectrophotometry (n = 6). Cyclic GMP level was measured by radioimmunoassay (n = 8). Guanylate cyclase and cyclic GMP-phosphodiesterase activities were determined in an additional set of control rats (n = 10). The cyclic GMP levels were not different between the ischaemic and contralateral areas in the control group. Compared to the cyclic GMP in the control ischaemic cortex, topical methylene blue significantly decreased the cyclic GMP level by 56% in the ischaemic cortex of the methylene blue group. Ischaemia did not alter the activities of guanylate cyclase but mildly decreased cyclic GMP-phosphodiesterase. The regional cerebral blood flow and O2 consumption in the control group were 50% and 32% lower than those in corresponding contralateral cortex. Topical methylene blue did not alter regional cerebral blood flow and O2 consumption in the ischaemic cortex. Our data showed that cyclic GMP is not a major controller on O2 supply or O2 consumption in the ischaemic brain.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1994

Effects of inhibition of nitric oxide synthase on blood-brain barrier transport in focal cerebral ischemia.

This study was performed to determine whether nitric oxide (NO) alters the transport of small hydrophilic molecules across the blood-brain barrier in focal cerebral ischemia by administering an NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) and by measuring the blood-brain barrier transfer coefficient (Ki) of 14C-alpha-aminoisobutyric acid (14C-AIB) in the rats with middle cerebral artery occluded under isoflurane anesthesia. L-NAME increased the mean arterial blood pressure from 91 +/- 9 to 134 +/- 13 mm Hg. The Ki of the ischemic cortex (ICO) was 26% higher than that of the contralateral cortex (CCO) in the control animals without the L-NAME treatment. However, in the L-NAME-treated animals, Ki was 33% lower in the ICO than in the CCO. The Ki of ICO in the L-NAME group was significantly lower (-54%) than that of the control group. L-NAME did not affect Ki significantly in the nonischemic brain regions. Our data demonstrate that focal ischemia increased Ki of 14C-AIB, but L-NAME significantly decreased the Ki in the focal ischemic area of the brain without causing significant changes in the nonischemic tissue. Our results suggest that NO may participate in increasing transport of small hydrophilic molecules across the blood-brain barrier in focal ischemia.

Amino Acid Oxidoreductases↗

PubMed1994

Nitric oxide synthase inhibition alters cerebral blood flow and oxygen balance in focal cerebral ischemia in rats.

BACKGROUND AND PURPOSE: This study investigated whether the nitric oxide synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) would alter blood flow and oxygen balance in the ischemic cerebrocortex of isoflurane-anesthetized Long-Evans rats. METHODS: Fifteen minutes after middle cerebral artery occlusion, L-NAME (1.5 mg/min per kilogram) was infused intravenously to the L-NAME group (n = 14), and normal saline was given to the control group (n = 14) for 45 minutes. In each group, regional cerebral blood flow was determined with [14C]iodoantipyrine, and arterial and venous oxygen saturations were determined by microspectrophotometry. RESULTS: In both groups regional cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex ([mean +/- SD] 55 +/- 13 versus 110 +/- 29 mL/min per 100 g in the control group and 35 +/- 13 versus 90 +/- 24 mL/min per 100 g in the L-NAME group). Compared with the blood flow in the ischemic cortex of the control group, L-NAME significantly reduced ischemic blood flow by 36%. Venous oxygen saturation was significantly increased in the ischemic cortex (41 +/- 1% versus 44 +/- 3%) but decreased in the contralateral cortex (65 +/- 3% versus 61 +/- 4%) by L-NAME. Calculated ischemic cortical oxygen consumption in the L-NAME group was 39% lower than that in the corresponding control group, whereas the difference was only 11% in the contralateral sides between groups. In both groups, the ratio of oxygen supply to consumption was lower in the ischemic than in the nonischemic regions. In the ischemic cortex, this ratio was significantly lower in the control group than in the L-NAME group (1.7 +/- 0.1 versus 1.9 +/- 0.1). In contrast, the ratio tended to be decreased by L-NAME in nonischemic regions. CONCLUSIONS: These observations suggest that despite a decrease in cerebral blood flow, inhibition of nitric oxide synthesis mildly improves the oxygen supply and consumption balance in the ischemic cortex.

Amino Acid Oxidoreductases↗

PubMed1994

Effect of ketamine on heterogeneity of cerebral microregional venous O2 saturation in the rat.

Heterogeneity of microregional O2 supply and consumption balance exists in the brain. Previous studies have shown that anesthetics such as pentobarbital and isoflurane, decrease the heterogeneity of O2 saturation in the small veins of the brain. This study was performed to determine whether ketamine, an anesthetic, would alter this heterogeneity. Rats were anesthetized with isoflurane for the cannulation of the femoral artery and vein. Ninety minutes after discontinuation of isoflurane, they either received injections with ketamine 100 mg/kg intraperitoneally (IP) (n = 7) or were used as conscious controls (n = 7). In each rat, regional cerebral blood flow (rCBF) was determined by 14C-iodoantipyrine autoradiography, and microregional arterial and venous (diameter 20-100 microns) O2 saturation was measured by microspectrophotometry in the anterior cortex, posterior cortex, and pons. The average rCBF and O2 consumption were similar between the two groups in each brain region except in the anterior cortex, where the O2 consumption of the ketamine group was slightly higher than that of the conscious animals. The average regional O2 supply-to-consumption ratios were similar in the three brain regions in both of the groups. However, there was heterogeneity of the O2 saturation in small veins in all the brain regions that we studied. The coefficient of variation [CV = (SD/mean X 100] of venous O2 saturation of the ketamine group in the anterior cortex (19.8 +/- 7.2), in the posterior cortex (18.8 +/- 9.4), and in the pons (16.7 +/- 6.5) was not significantly different from that in the conscious animals (22.8 +/- 6.4, 23.1 +/- 5.3, and 15.7 +/- 6.4, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Diminished effect of inhibition of nitric oxide synthase on regional cerebral vascular resistance in conscious and in isoflurane anesthetized rats during hemorrhage.

Effects of a nitric oxide (NO) synthase inhibitor on regional cerebral vascular resistance (rCVR) and regional cerebral blood flow (rCBF) were studied during a severe hemorrhage in conscious and in isoflurane anesthetized groups of rats. Half of each group was infused with NG-nitro-L-arginine-methyl ester (L-NAME), a NO synthase inhibitor, at a rate of 2 mg.kg-1.min-1 for 30 min. Half of the L-NAME infused and half of the normal saline infused rats were bled to reduce the mean arterial blood pressure (MAP) to 44-49 mmHg. rCBF was measured using [14C]iodoantipyrine. rCVR was calculated as the ratio of MAP to rCBF. In the conscious non-hemorrhagic rats, L-NAME markedly increased rCVR in all the brain regions that we studied. In the conscious rats without L-NAME treatment, hemorrhage decreased rCVR in most of the brain regions. With L-NAME treatment in this group, hemorrhage increased rCVR only in the rostral part of the brain. Isoflurane decreased rCVR in most of the brain regions except the cortical area. L-NAME markedly increased rCVR in all the brain regions that we studied in the isoflurane anesthetized rats. In the isoflurane anesthetized rats, hemorrhage did not reduce rCVR in any of the brain regions. In the isoflurane anesthetized hemorrhagic rats, L-NAME did not significantly affect rCVR in any of the brain regions that we studied. We found that L-NAME increased rCVR to a greater extent in the non-hemorrhagic rats than in the hemorrhagic rats in both the conscious and in the isoflurane anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗

PubMed1993

Effects of pentobarbital and isoflurane on regional cerebral oxygen extraction and consumption with middle cerebral artery occlusion in rats.

BACKGROUND: When compared with barbiturates, isoflurane may lack protective effects during focal cerebral ischemia. The reason for this difference is not clear. In this study, regional cerebral blood flow (rCBF), arterial and venous O2 saturation, and O2 extraction were compared in the ischemic cortex and in the nonischemic brain regions of rats anesthetized with isoflurane or pentobarbital using a microspectrophotometric technique that directly measures the O2 saturation of blood in the small arteries and veins. METHODS: Twenty-eight rats were anesthetized with 1.4% isoflurane or 50 mg/kg pentobarbital. One hour after a middle cerebral artery (MCA) occlusion, rCBF was measured in the ischemic cortex and in the nonischemic brain regions using 14C-iodoantipyrine in one-half of each group of animals. Regional arterial and venous O2 saturation were determined using microspectrophotometry in the other one-half of each group. RESULTS: The rCBF of the ischemic cortex (IC) and the non-ischemic contralateral cortex (CC) of the isoflurane group were significantly higher than those of the pentobarbital group. The venous O2 saturation was significantly less, and the O2 extraction was significantly higher, in the IC than in the nonischemic regions in both groups of animals (pentobarbital group, IC 10.5 +/- 1.1 ml O2.100 ml blood-1, CC 6.3 +/- 0.7; isoflurane group, IC 10.8 +/- 0.6, CC 5.9 +/- 0.2). There was no significant difference between the two groups. CONCLUSIONS: Because the rCBF was less and the O2 extraction was similar, O2 consumption in the focal ischemic area of the brain during pentobarbital anesthesia must have been less than that during isoflurane anesthesia.

Animals↗

PubMed1993

Effects of nitric oxide synthase inhibition on regional cerebral blood flow and vascular resistance in conscious and isoflurane-anesthetized rats.

Nitric oxide is an important regulator of the regional cerebral vascular tone. We compared the magnitude of nitric oxide-related changes in the vascular tone by studying the regional cerebral blood flow (rCBF) and vascular resistance in conscious and isoflurane-anesthetized rats by using a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). In the conscious group (n = 12), after cannulation of a femoral artery and two veins under isoflurane anesthesia, rats were allowed to remain awake for 90 min. In the anesthetized group (n = 18), rats were anesthetized with 2% isoflurane and mechanically ventilated. Six rats in each group were treated with L-NAME (2 mg.kg-1 x min-1 for 30 min) or saline. For the remaining rats in the isoflurane-anesthetized group (n = 6), arterial blood pressure was increased by phenylephrine infusion to the same level as that in the L-NAME-treated, isoflurane-anesthetized rats. Regional vascular resistance was determined by the ratio of mean arterial blood pressure and rCBF which was measured by [14C]iodoantipyrine. L-NAME significantly increased mean arterial blood pressure in both the conscious (123 to 158 mm Hg) and anesthetized (82 to 144 mm Hg) rats. Regional vascular resistance increased significantly in all 12 brain regions studied with the average value increasing from 1.19 +/- 0.33 mm Hg.mL-1 x min x 100 g to 2.22 +/- 0.48 (P < 0.0001) in the conscious and from 0.78 +/- 0.27 to 1.61 +/- 0.48 (P < 0.0001) in the isoflurane-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗

PubMed1992

Effect of pentobarbital on cerebral regional venous O2 saturation heterogeneity.

Observed venous O2 saturation inhomogeneity in the brain implies a microregional imbalance in O2 supply/consumption. We hypothesized that this heterogeneity should be decreased by pentobarbital anesthesia through a reduction in regional metabolic heterogeneity. Male, Long-Evans, approximately 350 g rats were either anesthetized with 50 mg/kg pentobarbital (n = 10) or used as a conscious control group (n = 10, catheters inserted two hours earlier under ether anesthesia). In each rat, regional cerebral blood flow was determined by [14C]iodoantipyrine and regional arterial and venous O2 saturation were determined by microspectrophotometry. In the PB group, the mean blood pressure (107 +/- 7 Torr), heart rate (362 +/- 29/min), average cerebral blood flow (63 +/- 19 ml/min/100 g), and average cerebral O2 consumption (3.7 +/- 1.2 ml O2/min/100 g) were lower than those values in the conscious group (128 +/- 15, 474 +/- 44, 112 +/- 40, and 7 +/- 3), respectively. O2 extraction did not change after pentobarbital anesthesia. However, the dispersion of venous O2 saturation narrowed. The distribution of O2 saturations in 373 cerebral veins of anesthetized rats had a significantly reduced coefficient of variation [C.V. = 100 x (S.D./mean) = 13] as compared to a C.V. of 18 in 320 veins in conscious rats. Thus, pentobarbital anesthesia reduced the microregional venous O2 saturation inhomogeneity in the brain, creating a more uniform balance of oxygen supply and consumption.

Animals↗

PubMed1992

Effects of isoflurane on transport across the blood-brain barrier.

The blood-brain barrier (BBB) plays an important role in regulating and restricting transfer of molecules into the interstitial space of the brain. Anesthetic agents may affect the permeability of the BBB. In this investigation, the effect of isoflurane on the transport of small hydrophilic molecules across the BBB was studied in rats by measuring the blood-brain transfer coefficient (Ki) and the regional cerebral blood flow (rCBF) and by calculating the capillary permeability-surface area (PS) product. In the control group, after a femoral artery and vein were catheterized under isoflurane anesthesia, rats were allowed to remain awake for 2 h before measuring Ki (n = 6) or rCBF (n = 11). In the two experimental groups, rats were anesthetized with 1% and 2% isoflurane respectively, and their lungs were mechanically ventilated through a tracheal tube. Ki was measured (1% n = 6, 2% n = 7) using 14C-alpha-aminoisobutyric acid, and rCBF was measured (2% n = 7) using 14C-iodoantipyrine. Two percent isoflurane did not affect rCBF in 9 of 13 brain regions. Blood flow was less in the lateral and posterior cortex and greater in the medulla and pons when compared with the control group. Ki was less in 11 of 13 brain regions in both the 1% and 2% isoflurane groups than in the control group. There was no significant difference between 1 and 2% isoflurane in any brain region.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗

PubMed1992

Effects of fentanyl on alpha-aminoisobutyric acid transfer across the blood-brain barrier.

The effect of fentanyl on the transfer of small hydrophilic molecules across the blood-brain barrier was studied in rats by measuring the blood-brain transfer coefficient (Ki) and the regional cerebral blood flow (rCBF) and by calculating the capillary permeability-surface area product. In the control group (n = 14), after a femoral artery and vein were catheterized under isoflurane anesthesia, the rats were allowed to remain awake for 1.5 h before measuring Ki (n = 8) using intravenous 14C-alpha-aminoisobutyric acid or rCBF (n = 6) using 14C-iodoantipyrine. In the fentanyl groups, rats were injected with 25 micrograms/kg (low (n = 6) or 100 micrograms/kg (high dose) of fentanyl (n = 14), followed by a continuous infusion at a rate of 50 or 200 micrograms.kg-1.h-1, respectively. Their lungs were mechanically ventilated. The Ki (low dose, n = 6; high dose, n = 8) and rCBF (high dose, n = 6) were measured 1 h after fentanyl infusion. The Ki was lower in 9 of 13 brain regions in the low-dose fentanyl group and in 7 of 13 brain regions in the high-dose fentanyl group than in the control animals. The average value of Ki in all the brain regions was 8.6 +/- 4.6 microL.g-1.min-1 in the control group, 5.2 +/- 2.9 microL.g-1.min-1 in the low-dose fentanyl group, and 5.7 +/- 2.9 microL.g-1.min-1 in the high-dose fentanyl group. High-dose fentanyl did not significantly affect rCBF in any brain region studied. The value of the regional permeability-surface area product was similar to the corresponding regional Ki in the groups studied. In conclusion, fentanyl decreased the transfer of small hydrophilic molecules across the blood-brain barrier, as demonstrated by a decreased Ki and permeability-surface area product, without significant changes in rCBF.

Aminoisobutyric Acids↗

PubMed1991

Effect of amphetamine on cerebral blood flow and capillary perfusion.

The purpose of this study was to determine the cerebral regional microvascular and vascular responses to amphetamine sulfate at a dose (5 mg/kg) known to affect neuronal function. Cerebral blood flow (14C-iodoantipyrine method) and percent of perfused capillaries (fluorescein isothiocyanate-dextran and alkaline phosphatase staining method) were determined during control and after intravenous administration of amphetamine in conscious Long-Evans rats. Amphetamine caused an increase in blood pressure (34%) and heart rate (31%). There was a significant increase in averaged cerebral blood flow from 98 +/- 8 to 166 +/- 9 ml/min/100 g after amphetamine. This flow increase was significant in the cortex, basal ganglia, pons and medulla, however the increase was not significant in the hypothalamus. In control rats, there were approximately 325 +/- 17 capillaries/mm2 of brain tissue and 52 +/- 1% of them were perfused. Amphetamine increased the percent perfused significantly to 72 +/- 1% in all examined regions. There was a similar significant increase in the percent of perfused cerebral capillary volume fraction. There were both vascular and microvascular responses to amphetamine, increasing cerebral blood flow as well as reducing the diffusion distance for oxygen.

Amphetamine↗

PubMed1991

Power spectral analysis of EEG during sufentanil infusion in humans.

The purpose of this study was to examine the relationship of continuous sufentanil infusion (0.71 micrograms.kg-1.min-1 for 14 min) and the response of the power spectrum of the electroencephalogram (EEG) performed during the induction of anaesthesia in 12 patients undergoing CABG surgery. Data were collected at various times including the preinduction period, every minute during the infusion period (minute 0 to 14), and 15, 20 and 25 min after the start of the infusion (1, 6 and 11 min respectively after completion of the infusion). Within three minutes of the sufentanil infusion, the total power and the relative power of delta increased to near maximum, while the 95% spectral edge and the mean frequency decreased markedly. In spite of the continued infusion of sufentanil, there were very little further changes in the EEG activity. This ceiling effect for the EEG changes appear to coincide with the failure to respond to verbal command. We conclude that the power spectrum of the EEG failed to respond to increasing doses of sufentanil during its infusion after the rapid initial changes.

Alpha Rhythm↗

PubMed1991

Effects of MK-801 on cerebral regional oxygen consumption in focal cerebral ischemia in rats.

This investigation tested in rats whether MK-801, an N-methyl-D-aspartate receptor antagonist, would improve the balance of oxygen supply and consumption in the focal ischemic area of the brain induced by occlusion of the middle cerebral artery. Fifteen minutes after middle cerebral artery occlusion, 5 mg/kg MK-801 was administered intravenously to the MK-801 group (n = 12), and normal saline was given to the control group (n = 12). One hour after the occlusion in each group, regional cerebral blood flow was determined in six rats using [14C]iodoantipyrine, and regional arterial and venous oxygen saturations were determined using a microspectrophotometric technique in the other six rats. In both groups of animals, the cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex (36 +/- 16 [SD] and 67 +/- 14 ml/min/100 g for the control group; 33 +/- 10 and 58 +/- 11 ml/min/100 g for the MK-801 group, respectively). Oxygen extraction was significantly higher in the ischemic cortex (8.8 +/- 2.1 ml O2/100 ml blood) than in the contralateral cortex (5.6 +/- 0.3) for the control group. However, for the MK-801 group, there was no significant difference between the ischemic cortex (6.1 +/- 1.0) and the contralateral cortex (5.7 +/- 1.1). Oxygen extraction in the ischemic cortex of the MK-801 group was significantly lower than that of the control group. Calculated ischemic regional oxygen consumption was similar to the nonischemic values in the control group, whereas the ischemic value was reduced to 61% of the value of the contralateral cortex in the MK-801 group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Visual evoked potentials during etomidate administration in humans.

The effects of etomidate on visual evoked potentials (VEP) were studied in 22 patients undergoing gynaecological procedures. They were divided into two groups: the etomidate group (12 patients) and the fentanyl-N2O-etomidate group (ten patients). In the etomidate group, etomidate 0.3 mg.kg-1 was given as a bolus injection during induction of anaesthesia which was followed by an infusion of etomidate 0.05 mg.kg-1.min-1. No significant changes were observed in the amplitudes of P100 or N70. Latencies of the P60, N70, and P100 were slightly increased. In the fentanyl-N2O-etomidate group, a bolus injection of 0.3 mg.kg-1 of etomidate was given during anaesthesia with 3-4 micrograms.kg-1 of fentanyl and 60 per cent nitrous oxide. The amplitude of the P100 was significantly decreased and the latencies of the P60 and N70 were significantly increased. In conclusion, interpretation of the VEP during etomidate administration alone was not hard to perform but, when given together with fentanyl-nitrous oxide anaesthesia, the VEP was affected significantly making its interpretation difficult.

Adult↗